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METTL16 drives leukemogenesis and leukemia stem cell self-renewal by reprogramming BCAA metabolism

ABSTRACT: METTL16 drives leukemogenesis and leukemia stem cell self-renewal by reprogramming BCAA metabolism

PROVIDER: PRJNA785622 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17095403.fastq.gz	Fastqsanger.gz
	SRR17095404.fastq.gz	Fastqsanger.gz
	SRR17095405.fastq.gz	Fastqsanger.gz
	SRR17095406.fastq.gz	Fastqsanger.gz
	SRR17095407.fastq.gz	Fastqsanger.gz

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RNA-seq in wild-type, METTL16-knockout, and METTL16 rescue NOMO-1 cells

Project description:METTL16 belongs to methyltransferase like (METTL) family and could install m6A marks on its substrates. Here, we uncover a tumor-promoting role of METTL16 in AML and LSC self-renewal. To explore the mechanism underlying the oncogenic function of METTL16 in AML, we performed m6A-seq and RNA-seq. Via integrated analysis of m6A-seq data and RNA-seq data, we identified two bona fide targets of METTL16, BCAT1 and BCAT2. METTL16 functions as an m6A methyltransferase to regulate expression of BCAT1 and BCAT2, which contribute to reprogramming BCAA metabolism.

2023-01-12 | GSE190044 | GEO

METTL16 drives leukemogenesis and leukemia stem cell self-renewal by reprogramming BCAA metabolism.

Project description:N6-methyladenosine (m6A), the most prevalent internal modification in mammalian mRNAs, is involved in many pathological processes. METTL16 is a recently identified m6A methyltransferase. However, its role in leukemia has yet to be investigated. Here, we show that METTL16 is a highly essential gene for the survival of acute myeloid leukemia (AML) cells via CRISPR-Cas9 screening and experimental validation. METTL16 is aberrantly overexpressed in human AML cells, especially in leukemia stem cells (LSCs) and leukemia-initiating cells (LICs). Genetic depletion of METTL16 dramatically suppresses AML initiation/development and maintenance and significantly attenuates LSC/LIC self-renewal, while moderately influencing normal hematopoiesis in mice. Mechanistically, METTL16 exerts its oncogenic role by promoting expression of branched-chain amino acid (BCAA) transaminase 1 (BCAT1) and BCAT2 in an m6A-dependent manner and reprogramming BCAA metabolism in AML. Collectively, our results characterize the METTL16/m6A/BCAT1-2/BCAA axis in leukemogenesis and highlight the essential role of METTL16-mediated m6A epitranscriptome and BCAA metabolism reprograming in leukemogenesis and LSC/LIC maintenance.

| S-EPMC9838187 | biostudies-literature

Determine the methyltransferase activities of METTL16 via MeRIP-seq (m6A-seq)

2023-01-12 | GSE189995 | GEO

METTL16 drives leukemogenesis and leukemia stem cell self-renewal by reprogramming BCAA metabolism

Project description:This SuperSeries is composed of the SubSeries listed below.

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Asymmetric self-renewal associated (ASRA) genes

Project description:Cell lines geneticially engineered to undergo conditional asymmetric self-renewal were used to identify genes whose expression is asymmetric self-renewal associated (ASRA). Non-random sister chromatid segregation occurs concordantly with asymmetric self-renewal in these cell lines. Asymmetric self-renewal occurs when murine embryo fibroblasts that are otherwise p53-null are induced to express physiological levels of wildtype p53 protein (Asym). To distinguish p53-responsive genes that also require induction of asymmetric self renewal (i.e., ASRA genes) and/or non-random sister chromatid segregation for change, an additional control cell line, which continues to symmetrically self-renew (with random sister chromatid segregation) even when p53 is induced, was also compared (Symp53). This congenic cell line constitutively expresses the type II inosine monophosphate dehydrogenase (IMPDH II; the rate-limiting enzmye for guanine ribonucleotide biosynthesis) and, thereby, prevents p53-induced asymmetric self-renewal and non-random sister chromatid segregation. Three biological replicates of asymmetrically self-renewing cultures (Asym1-3) were compared with cultures that were symmetrically self-renewing - either because they did not express p53 (3 biological replicates, Sym1-3) or they expressed constitutive IMPDH II (i.e., not regulated by p53) as well as p53 (2 biological replicates, Symp53_1 and 2.)

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Asymmetric self-renewal associated (ASRA) genes

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Enforcement of stem-cell dormancy by NPMc+ is a critical determinant of unrestricted self-renewal during myeloid leukemogenesis

Project description:Enforcement of stem-cell dormancy by NPMc+ is a critical determinant of unrestricted self-renewal during myeloid leukemogenesis

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Enforcement of stem-cell dormancy by NPMc+ is a critical determinant of unrestricted self-renewal during myeloid leukemogenesis

Project description:Enforcement of stem-cell dormancy by NPMc+ is a critical determinant of unrestricted self-renewal during myeloid leukemogenesis

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Enforcement of stem-cell dormancy by NPMc+ is a critical determinant of unrestricted self-renewal during myeloid leukemogenesis

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2022-08-10 | GSE157702 | GEO

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